In episode 25, Insulin Resistance Isn’t All About Carbs and Insulin, I explained why an individual cell would “decide” to stop taking up energy. Here in episode 26, I explain tissue-level energy overload, focusing on adipose tissue and liver.
At adipose tissue, the problem with fatness isn’t the amount of fat. It’s that we’ve reached the point where we can’t get any fatter. Well, we can, but we can no longer do so while maintaining a healthy organizational structure within adipose tissue that allows blood, oxygen, and nutrients to get to where they need to go. Surprisingly, some of the things that enable proper expansion, and thus protect our metabolic health, are things that we usually think of as “bad,” such as inflammation. In fact, the pro-inflammatory changes in the gut microbiome in response to an obesogenic diet provide information to adipose tissue that it needs to prepare for healthy expansion. And adipose expansion is most protective at the site of the “bad” body fat: visceral fat in the abdomen.
At liver, the problem is fat gets trapped in the liver, flattening out everything in the cell and hogging the space needed for glycogen storage, and this can happen even in a lean person.
I conclude with some practical recommendations about body composition and nutrient density.
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Read on for the show notes.
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Show Notes for Episode 26
In this episode, you will find all of the following and more:
09:40 Cliff Notes
13:08 Mechanics of adipose tissue expansion
15:40 Consequences of poor adipose tissue expansion
17:12 Internal Stress as a consequence
19:47 Animal models of limitations to adipose expansion
24:12 Glycerol availability manipulated by PEPCK expression
27:20 Carbohydrate could play a role in preventing metabolic dysfunction by providing glycerol if glyceroneogenesis is limiting
28:05 Deletion of genes involved in lipid droplet formation
28:42 Septa organization
29:02 Deletion of collagen genes
29:53 Matrix metalloproteinases (MMPs)
31:11 Hypoxia and HIF1 – alpha
32:15 Inflammation (tumor necrosis factor alpha or TNF -alpha, interleukins or ILs toll-like receptors or TLRs) is necessary to allow proper extracellular matrix (ECM) reorganization and capillary bed reorganization
36:58 Visceral abdominal fat expansion is most protective because visceral fat drains directly into the liver via the portal vein, and releases more fat into the liver when it cannot expand further
41:48 Liver as the metabolic hub of fat and carbohydrate metabolism
43:45 Fat accumulation in liver likely directly compromises glycogen storage
48:45 Factors in fatty liver disease
50:45 Sources of liver fat: adipose, dietary fat, de novo lipogenesis (DNL) from carbohydrate is minor
57:08 Factors in triglyceride export: oxidative stress and choline
59:08 The choline requirement is increased more by fat than other macronutrients and more by long-chain saturated fats than other fats
1:04:54 Practical strategies: body composition is king and queen, but it might not be the right time to lose fat
1:06:28 A well rounded nutrient-dense diet is low-hanging fruit at any time
1:10:44 Additional strategies require nutritional analysis with the help of a health care professional and data generation
Links and Research Related to Episode 26
Episode 25 on what causes insulin resistance in an individual cell.
Start Here for Fatty Liver Disease (and index of my related posts)
Episode 3 on The Sugar Conspiracy
Episode 23 on how I lost 30 pounds in four months, how I knew it was time, why it sometimes isn’t the right time to lose weight, and how to make it time.
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